Monkey breeders (M. nemestrina) at high or low risk for offspring mortality, prematurity, and low birth weight were mated and subjected to high or low prenatal stress. High risk females aborted regardless of stress (68%), low risk stressed also aborted (50%), unstressed low risk females had a low abortion rate of 7%. Less lipid and fewer lesions occurred in brains of healthy newborns compared with stillborns or deaths from respiratory distress. Low birth weight was related to anomalies in growth, feeding, diurnal cycles, and other aspects of behavior. Correlates of human offspring mortality, prematurity, and abnormal development also appeared for monkeys. Also, abortion and stillbirth on one pregnancy were followed by even higher rates on the next, and induced abortion was followed by a very high spontaneous abortion rate. Thus, research on this experimental model should identify genetic, prenatal, and perinatal factors which result in offspring mortality, prematurity, and mental retardation or other disabilities, with the goal of prevention of bad pregnancy outcomes and consequent offspring abnormality. To approach this goal we propose experiments having the following aims. A: Identify specific factors causing abortions. Prevent abortions and produce spontaneous premature survivors. Also produce prematurity by C-section to eliminate mechanical birth trauma effects. Identify abnormalities produced by parental risk and prenatal stress interacting with perinatal trauma and rearing under environmental stimulus deprivation. B: Assess effects of induced abortion on the next pregnancy. C: Identify effects of intrusive medical intervention on prematures, and determine beneficial or harmful effects of adding extra stimulation in a high risk nursery. D: Determine causes of neonatal death in young primipara (45%), and stillbirths in aged, high parity, mothers (40%). E: Relate cytogenetic, serological, infection, fertility, endocrine, and brain pathology findings to offspring abnormalities occurring in all experiments.